The medium chain acyl-CoA dehydrogenase (MCAD) is the best known structure of all ACADs, and is the most commonly deficient enzyme within the class that leads to metabolic disorders in animals. [1]

Jun 5, 2024 · Crystal structures of human long-chain acyl-CoA dehydrogenase (LCAD) and the catalytically inactive Glu291Gln mutant, have been determined. These structures suggest that LCAD harbors...

Jan 3, 1997 · Long chain acyl-CoA dehydrogenase (LCAD) catalyzes the first step in the β -oxidation spiral. Our objective was to define regulatory elements of the human LCAD gene required for high levels of expression in mature heart and to locate elements suppressing gene expression in the fetus.

Long-chain acyl-CoA dehydrogenase (LCAD) is a mitochondrial flavoenzyme thought to be one of the major enzymes responsible for the first step of long-chain fatty acid (LCFA) β-oxidation. Surprisingly, recent studies have shown LCAD is hardly …

May 31, 2000 · Their names, short-chain acyl-CoA dehydrogenase (SCAD), medium-chain acyl-CoA dehydrogenase (MCAD), long-chain acyl-CoA dehydrogenase (LCAD), and very long-chain acyl-CoA dehydrogenase (VLCAD), reflect the acyl chain lengths of their preferred substrates.

Sep 1, 2019 · Here, we established that the mitochondrial flavoprotein long-chain acyl-CoA dehydrogenase (LCAD), which catalyzes a key step in mitochondrial FAO, directly produces H 2 O 2 in vitro by leaking electrons to oxygen.

Dec 22, 1998 · To evaluate the functional role of LCAD in mitochondrial FAO in vivo, we developed a mouse model of LCAD deficiency by targeted mutagenesis of the gene encoding LCAD (Acadl) in mouse embryonic stem (ES) cells.

The two samples of infant lung with no detectable LCAD were both positive for MCAD, a closely related enzyme to LCAD, as well as surfactant protein-B expression demonstrating the presence of ATII cells in the archived lung materials (Fig. 8 a, bottom panel).

Long-chain acyl-CoA dehydrogenase (LCAD), encoded by the ACADL gene, is one of four mitochondrial acyl-CoA dehydrogenases (ACADs) that catalyze the first enzymatic step in fatty acid β-oxidation (FAO).

We report here a previ-ously unappreciated mechanism by which HIF-1 suppresses the medium-chain (MCAD) and long-chain (LCAD) acyl-CoA dehy-drogenases and FAO to facilitate cancer progression by cross-talk between metabolic and signal transduction pathways.